Many researches are directed to organ lesions caused by various toxicants and drugs. In daily life, various toxicants mainly enter into human body via respiratory tract, skin and digestive tract, and result in multi-system and organ lesions. There are many injury mechanisms. In lead poisoning, lead as a poly-affinity toxicant acts on all systems of body, and mainly injures nerve system, hematopoietic system, digestive system and cardiovascular system, wherein the most important injury is the metabolism disorder of porphyrin, an intermediate product during the synthesis of hemoglobin. In mercury poisoning, mercury ion binds to mercapto groups of enzymes in vivo, and thus inhibits the activity of enzymes and blocks the normal metabolism of cells, which further cause central nerve and autonomic nerve dysfunctions of central nerve and autonomic nerve and lesions of digestive tract and kidney. In poisoning of arsenic and compounds thereof, arsenic and oxides thereof bind to mercapto groups of cellular enzymes in vivo, in particular, they bind to the mercapto group of pyruvate oxidase and inactivate this enzyme, which affect normal metabolism of cells and firstly result in lesions of nerve system and blood capillary, so that human body exhibits toxic symptoms. In methanol poisoning, methanol mainly acts on central nerve system and brings about a selective toxic effect, and the toxic symptoms are similar to alcoholism but more serious. Methanol destroys intracellular oxidization, so that the accumulation of lactic acid and other organic acids causes acid poisoning. Cyanide poisoning causes oxidization disorder in body, which results in so-called “intracellular choke”. Although there are various toxicosis mechanisms, most of them relate to effects of cellular level on redox reactions during the metabolism process, or effects that toxicants act directly as oxidants, or effects that toxicants destroy activity of enzymes.
In drug poisoning, barbiturate poisoning mainly results in the inhibition of central nerve system, the most prominent toxic effect of chloropromazine is extrapyramidal motor system dysfunction which exhibits muscle convulsion, akathisia, etc. These symptoms cannot be healed for a long time after drug withdrawal.
At present, therapeutics for treating toxicosis of drugs and toxicants include: intravenous injection of 10% calcium gluconate, 1-2 times per day, for 2-3 days, deleading therapy with sodium dimercaptosuccinate, de-arsenicing therapy with dimercaptopropanol, or gastrolavage; gastrolavage with sodium hydrogen carbonate or peritoneal dialysis for treating methanol poisoning; therapy for treating cyanide poisoning by using sodium thiosulfate, or glucose, or dicobalt edetate in combination with glucose. In general, said therapeutics are at the level of competitive binding, quick dilution, concentration decrease and damage reduction, and there is essentially not therapeutics that has said functions and can act against toxicants and drugs at sites of toxic action in order to eliminate the toxic effect fundamentally.
N-acetyl-D-glucosamine is a chemical reagent. From the 1990's, it is continually used to treat diseases such as pericementitis (WO9102530A1), microbiological infection (WO9718790A3), intestinal inflammation (WO9953929A1), cornea disease (JP10287570A2), hypertrophy of the prostate (U.S. Pat. No. 5,116,615), and so on. It is also applied in cosmetology (JP59013708A2), shampoo preparation (JP2011505A2), and the like, but it has not been used in the manufacture of a medicament for treating organ lesions caused by toxicosis of drugs or toxicants.
The inventor of the present invention finds that N-acetyl-D-glucosamine and pharmaceutically acceptable salts can rapidly and effectively treat toxic reactions of drugs and toxicants, competitively bind to toxicants to convert toxicants into nontoxic substances, reduce oxidation-type toxicants to alleviate their toxic effects on cell components, and form a dynamically changed isogeneric action barrier on surface of cells and bio-macromolecules to eliminate and segregate toxic effects, thereby the present invention is carried out.